W2041 Effects of the Nitric Oxide (NO) Synthase Inhibitor, NG-Nitro-L-Arginine-Methyl-Ester (L-NAME), On Delayed Gastric Emptying Induced By Hyperglycaemia in Healthy Humans

2009 ◽  
Vol 136 (5) ◽  
pp. A-779
Author(s):  
Paul Kuo ◽  
Diana Gentilcore ◽  
Nivasinee Nair ◽  
Julie E. Stevens ◽  
Odd Helge Gilja ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Gastric Emptying ◽  
Methyl Ester ◽  
Delayed Gastric Emptying ◽  
No Synthase ◽  
Healthy Humans ◽  
No Synthase Inhibitor ◽  
Synthase Inhibitor

scholarly journals Role of Nitric Oxide in Regulating Cerebrocortical Oxygen Consumption and Blood Flow during Hypercapnia

1994 ◽  
Vol 14 (3) ◽  
pp. 503-509 ◽  
Author(s):  
Ildiko Horvath ◽  
Norbert T. Sandor ◽  
Zoltan Ruttner ◽  
Alan C. McLaughlin
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Methyl Ester ◽  
Superior Sagittal Sinus ◽  
No Synthase ◽  
Sagittal Sinus ◽  
No Synthase Inhibitor ◽  
Synthase Inhibitor

The effect of the nitric oxide (NO) synthase inhibitor Nω-nitro-l-arginine methyl ester (l-NAME) on the response of cerebrocortical oxygen consumption (CMRO2) and blood flow (CBF) to two levels of hypercapnia (Paco2 ∼ 60 mm Hg and Paco2 ∼ 90 mm Hg) was investigated in ketamine-anesthetized rats. CBF was calculated using the Kety–Schmidt approach and CMRO2 was calculated from the product of CBF and the arteriovenous (superior sagittal sinus) difference for oxygen. l-NAME treatment did not have a significant effect on either CMRO2 or CBE under normocapnic conditions but inhibited the hypercapnic increase of CMRO2 and the hypercapnic increase in CBF. These results suggest that NO plays a role in the response of CMRO2 and CBF during hypercapnia and are consistent with the suggestion that at least part of the increase in CBF observed during hypercapnia is coupled to an increase in CMRO2.

scholarly journals Downregulation of nNOS and synthesis of PGs associated with endotoxin-induced delay in gastric emptying

2002 ◽  
Vol 283 (6) ◽  
pp. G1360-G1367 ◽  
Author(s):  
Sara Calatayud ◽  
Eugenia García-Zaragozá ◽  
Carlos Hernández ◽  
Elsa Quintana ◽  
Vicente Felipo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Gastric Emptying ◽  
Methyl Ester ◽  
Intraperitoneal Injection ◽  
Delayed Gastric Emptying ◽  
Single Intraperitoneal Injection ◽  
Inos Inhibitor ◽  
Oxide Synthase ◽  
Experimental Group ◽  
Inducible Nos

A single intraperitoneal injection of endotoxin (40 μg/kg) significantly delayed gastric emptying of a solid nutrient meal. Blockade of nitric oxide synthase (NOS) with 30 mg/kg ip N G-nitro-l-arginine methyl ester or 20 mg/kg ip 7-nitroindazole [neuronal NOS (nNOS) inhibitor] significantly delayed gastric emptying in control animals but failed to modify gastric emptying in endotoxin-treated rats. Administration of 2.5, 5, and 10 mg/kg ip N 6-iminoethyl-l-lysine [inducible NOS (iNOS) inhibitor] had no effect in either experimental group. Indomethacin (5 mg/kg sc), NS-398 (cyclooxygenase-2 inhibitor; 10 mg/kg ip), and dexamethasone (10 mg/kg sc) but not quinacrine (20 mg/kg ip) significantly prevented delay in gastric emptying induced by endotoxin but failed to modify gastric emptying in vehicle-treated animals. Ca2+-dependent NOS activity in the antrum pylorus of the stomach was diminished by endotoxin, whereas Ca2+-independent NOS activity was not changed. In addition, decreased nNOS mRNA and protein were observed in the antrum pylorus of endotoxin-treated rats. Our results suggest that downregulation of nNOS in the antrum pylorus of the stomach and synthesis of prostaglandins mediate the delay in gastric emptying of a solid nutrient meal induced by endotoxin.

ANESTHETIC ACTION OF ETOMIDATE IS ENHANCED BY THE NO-SYNTHASE INHIBITOR NITRO-L-ARGININE-METHYL-ESTER (L-NAME)

1998 ◽  
Vol 89 (Supplement) ◽  
pp. 180A
Author(s):  
T. Krause ◽  
P. H. Tonner ◽  
J. Scholz ◽  
E. Suppe ◽  
J. Schulte Esch
Keyword(s):  
Methyl Ester ◽  
No Synthase ◽  
No Synthase Inhibitor ◽  
Anesthetic Action ◽  
Synthase Inhibitor

Effect of l-NAME on oxygen uptake kinetics during heavy-intensity exercise in the horse

2001 ◽  
Vol 91 (2) ◽  
pp. 891-896 ◽  
Author(s):  
Casey A. Kindig ◽  
Paul McDonough ◽  
Howard H. Erickson ◽  
David C. Poole
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Electron Transport Chain ◽  
Slow Component ◽  
Oxygen Uptake Kinetics ◽  
No Synthase ◽  
Metabolic Rates ◽  
Transport Chain ◽  
Synthase Inhibitor ◽  
Reduced Time

There is evidence that oxidative enzyme inertia plays a major role in limiting/setting the O2 uptake (V˙o 2) response at the transition to higher metabolic rates and also that nitric oxide (NO) competitively inhibits V˙o 2 within the electron transport chain. To investigate whether NO is important in setting the dynamic response of V˙o 2 at the onset of high-intensity (heavy-domain) running in horses, five geldings were run on a treadmill across speed transitions from 3 m/s to speeds corresponding to 80% of peak V˙o 2with and without nitro-l-arginine methyl ester (l-NAME), an NO synthase inhibitor (20 mg/kg; order randomized). l-NAME did not alter (both P> 0.05) baseline (3 m/s, 15.4 ± 0.3 and 16.2 ± 0.5 l/min for control and l-NAME, respectively) or end-exerciseV˙o 2 (56.9 ± 5.1 and 55.2 ± 5.8 l/min for control and l-NAME, respectively). However, in the l-NAME trial, the primary on-kinetic response was significantly ( P < 0.05) faster (i.e., reduced time constant, 27.0 ± 2.7 and 18.7 ± 3.0 s for control andl-NAME, respectively), despite no change in the gain ofV˙o 2 ( P > 0.05). The faster on-kinetic response was confirmed independent of modeling by reduced time to 50, 63, and 75% of overallV˙o 2 response (all P < 0.05). In addition, onset of the V˙o 2 slow component occurred earlier (124.6 ± 11.2 and 65.0 ± 6.6 s for control and l-NAME, respectively), and the magnitude of the O2 deficit was attenuated (both P < 0.05) in the l-NAME compared with the control trial. Acceleration of the V˙o 2kinetics by l-NAME suggests that NO inhibition of mitochondrial V˙o 2 may contribute, in part, to the intrinsic metabolic inertia evidenced at the transition to higher metabolic rates in the horse.

Peculiarities of influence of NO-synthase inhibitors on behavioral parameters of rats

2020 ◽  
Vol 28 (3) ◽  
pp. 275-282
Author(s):  
Valentina G. Bashkatova ◽  
Natalia G. Bogdanova ◽  
Elena V. Alexeeva ◽  
Galina A. Nazarova ◽  
Sergey K. Sudakov
Keyword(s):  
Nitric Oxide ◽  
Locomotor Activity ◽  
Motor Activity ◽  
Pain Sensitivity ◽  
Selective Inhibitor ◽  
No Synthase ◽  
Anxiety Level ◽  
Male Rats ◽  
No Synthase Inhibitor ◽  
Synthase Inhibitor

Aim. A comparative study of the influence of nitric oxide synthase (NO-synthase) inhibitors on the parameters of anxiety, motor activity and pain sensitivity of rats. Materials and Methods. The work was conducted on male rats of Wistar line. The anxiety level and locomotor activity of rats were studied in the elevated plus maze (EPM) test. Pain sensitivity of the animals was tested on the hotplate apparatus. In the work, selective inhibitor of inducible isoform of NO-synthase aminoguanidine at a dose of 50 mg/kg, and non-selective inhibitor of this enzyme N-nitro-L-arginine at a dose of 50 mg/kg, were used. Rats of the control group were introduced the equivalent quantity of normal saline. NO-synthase inducible inhibitor aminoguadinine did not produce any influence on the anxiety level, but led to reduction of the horizontal motor activity of rats. Introduction of non-selective NO-synthase inhibitor N-nitro-L-arginine was accompanied by reduction of the anxiety and of the locomotor activity of animals in the EPM test. Both investigated NO-synthase inhibitors induced alteration of pain sensitivity of rats in the form of hypoalgesia. Here, the most pronounced nociceptive effect was observed with introduction of non-selective NO-synthase inhibitor. Conclusion. In the work the evidence of participation of inducible isoform of NO-synthase in realization of the motor activity and pain sensitivity processes in rats is shown. In result of the conducted experiments it was found that introduction of non-selective NO-synthase inhibitor N-nitro-L-arginine was accompanied by evident alterations of anxious behavior, locomotor activity and nociceptive sensitivity of rats. The results obtained confirm the important role of the system of regulation of nitric oxide synthesis in neurochemical mechanisms of behavioral reactions in rats.

A nitric oxide (NO) synthase inhibitor accelerates amygdala kindling

Neuroreport ◽  
1992 ◽  
Vol 3 (9) ◽  
pp. 805-808 ◽  
Author(s):  
Gérard Rondouin ◽  
Mireille Lerner-Natoli ◽  
Olivier Manzoni ◽  
Mireille Lafon-Cazal ◽  
Joel Bockaert
Keyword(s):  
Nitric Oxide ◽  
No Synthase ◽  
No Synthase Inhibitor ◽  
Amygdala Kindling ◽  
Synthase Inhibitor
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